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- W2027861665 abstract "We investigated whether or not acetylcholine elicited an endothelium-dependent contraction and whether an arachidonic acid metabolite was involved in the acetylcholine-induced contraction in ring preparations of rat renal arteries. Acetylcholine (0.1–100 μM) caused a transient contraction in endothelium-intact arteries in a concentration-dependent manner. The contraction induced by acetylcholine (10 μM) was enhanced by pretreatment with NG-nitro-l-arginine (100 μM), a nitric oxide synthase inhibitor, and was abolished by mechanical removal of the endothelium. Atropine (0.1 μM), quinacrine (1 and 3 μM), manoalide (0.1 and 1 μM), aspirin (1 and 10 μM), indomethacin (30 and 300 nM), ONO-3708 (9,11-dimethyl-methane-11,12-methano-13,14-dihydro-13-aza-14-oxo-15(β)-cyclophenyl-ω-pentenor-thromboxane A2l-arginine salt) (10 nM), S-1452 (calcium (5Z)-1R,2S,3S,4S-7-[3-phenylsulphonyl-aminobicyclo[2.2.1]hept-2yl]-5-heptenoate hydrate) (3 nM) and SQ29,548 ([1S-[1α,2β(5Z),3β,4α]]-7-[3-[[2-[(phenylamino) carbonyl]hydrazino]methyl]-7-oxabicyclo[2.2.1]hept-2-yl]-5-heptenoic acid) (3 and 10 nM), but not hexamethonium (1 μM), OKY-046 (sodium (E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid hydrochloride monohydrate) (100 μM) and CS-518 (sodium 2-(1-imidazolylmethyl)-4,5-dihydrobenzo[b]thiophene-6-carboxylate) (10 μM) significantly attenuated the acetylcholine (10 μM)-induced endothelium-dependent contractions in renal arteries pretreated with NG-nitro-l-arginine. These findings suggest that acetylcholine causes endothelium-dependent contraction by stimulation of muscarinic receptors in rat renal arteries, and that an arachidonic acid metabolite(s) of the cyclooxygenase pathway is involved in this endothelium-dependent contraction." @default.
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- W2027861665 date "1995-03-01" @default.
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- W2027861665 title "Endothelium-dependent contraction induced by acetylcholine in isolated rat renal arteries" @default.
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- W2027861665 doi "https://doi.org/10.1016/0014-2999(95)00023-e" @default.
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